We propose to define the effect of acute and chronic alcohol consumption on human host defense mechanisms. It is known that migration of granulocytes into areas of inflammation is impaired in states of acute intoxication: however, we will study patients chronically inebriated, and also perform in vitro tests of chemotaxis, to define the mechanism of this poor inflammatory response. Phagocytosis and killing of bacteria by granulocytes will also be studied in vitro, looking for cellular and/or humoral defects. Granulocyte kinetics, with and without inflammatory challenge, will be evaluated with radioactive tagging, as the mechanism of granulocytopenia in infected alcoholics remains obscure. In addition, we will study both in vivo and in vitro parameters of cell-mediated immunity, since clinical evidence has suggested defects in lymphocyte-dependent defense. We will avoid patients with documented cirrhosis, since a humoral inhibitor of lymphocyte transformation has been described in them. We propose to study alcoholic patients in two environments: 1) in the setting of acute infection - here are anticipated the most severe degrees of host defense impairment, but with the highest number of complicating variables; 2) in a controlled environment (CRC) with defined alcohol intake and diet - here the "pure" effects of alcohol on host defense mechanisms can be measured. BIBLIOGRAPHIC REFERENCES: Spagnuolo, P.J., and MacGregor, R.R., Ethanol effect on chemotaxis and other components of host defense, J. Lab. Clin. Med., 86:24-31, 1975. MacGregor, R.R., Relationship between granulocyte adherence and granulocyte kinetics, Clin. Res., 23:308A, 1975.